No abstract

Rat stomach sensitivity to pentagastrin was examined in fetal (days 19--21) and newborn (5--day-old) preparations in vivo and in vitro. Gastric acidification in vivo was expressed as the gastric content pH and in vitro as the net transepithelial H+ fluxes determined in an Ussing chamber. In both preparations, fetal stomach first responded to pentagastrin on day 20. Dose-dependent H+ secretion was demonstrated in vitro for pentagastrin concentrations of 10(-8) to 10(-6) M, with half-maximal stimulations at 1.9 x 10(-7) and 4 x 10(-7) M on days 20 and 21, respectively. In contrast, isolated fundic mucosa of 5-day-old rat pups exhibited very low H+ secretion rates, and pentagastrin did not significantly stimulate acid output. Fetal serum immunoreactive gastrin was detected as early as day 16 in fairly constant concentrations (about 77.5 pg eq synthetic human gastrin/ml). These results indicate that, although immunoreactive gastrin is present in serum as early as day 165, pentagastrin does nt stimulate acid secretion until day 20 when fetal stomach exhibits active H+ secretion and decreased passive permeability. Pentagastrin sensitivity disappears during the 1st days of extrauterine life. These findings strongly suggest that the development of pentagastrin sensitivity in rat stomach is biphasic.

In vivo fetal rat stomach produces HCl 48 h before birth. This study examines the mechanisms of H+ secretion from days 19 to 21 before birth. Isolated fetal stomachs were mounted as flat sheets in Ussing chambers for measurement of the transepithelial H+ fluxes (JH+) and short-circuit current (Isc), as indexes of the active ionic fluxes, and for measurement of total ionic conductance (G) and unidirectional mannitol fluxes from serosa to mucosa (JMans leads to m), as indexes of passive permeability. The results indicate that JH+ was absent at day 19 but reached 0.75 +/- 0.1 and 0.75 +/- 0.09 mueq . h-1 . cm-2 at days 20 and 21, respectively. Concomitantly, Isc increased significantly (56%) between days 19 and 20 in the direction of anion secretion or cation absorption. Parallel reductions in G (45%) and in JMans leads to m (66%) were observed between days 19 and 20. In conclusion, the simultaneous appearance of active H+ secretion and decreased passive transepithelial permeability strongly suggests that both processes are involved in the mechanism of acidification of the fetal rat stomach before birth.

The comparative growth patterns of endocrine gastrin and somatostatin cell populations were examined in the rat, during the perinatal period, to investigate possible relationships between their development and that of gastric acid secretion, gastrin and somatostatin hormones being implicated in the regulation of acid secretion. Total cell populations were estimated daily in the pancreas, stomach, and duodenum, by using a quantitative morphological method, from 19 days postcoitum to 8 days postpartum. In the pancreas, both cell types were present at 19 days postcoitum. After increasing, gastrin cells abruptly dropped from 4 days postpartum, while somatostatin cells continued to increase. In the stomach, gastrin cells seemed to appear at 19 days postcoitum, increasing with age. Somatostatin cells appeared only after birth and could be precisely quantified from 4 days postpartum. In the duodenum, the two cell types were present in similar numbers at 19 days postcoitum and increased similarly with age. Comparison of gastrin and somatostatin cell developmental behavior with previous data on the ontogeny of acid secretion shows a parallelism between the appearance of basal H+ fluxes at 20-21 days postcoitum and the high daily multiplication of the gastrin cell number in the three organs. Additionally, the marked decrease of pancreatic gastrin cell population at 4 days postpartum and the simultaneous development of the gastric somatostatin cell population might explain, among other mechanisms, the diminution of gastric acid secretion noted after birth.